The Impact of Longterm Exposure To Low Levels of Inorganic Arsenic on the Hypomethylation of Sept9 Promoter in Epithelialmesenchymal Transformed Colorectal Cancer Cell Lines

<div style=textalign: justify;>inorganic arsenicals are worldwide environmental contaminants that affect molecular characteristics in biological systems and lead to genomic and epigenomic instability as well as epithelial mesenchymal transition (emt). in this study, we aimed to investigate whether low levels of sodium arsenite (iasiii) can influence emt and genomic instability through microsatellite analysis. we have also determined epigenomic instability by investigating the methylation status of <em>sept9 </em>tumor marker in colorectal cancer (crc) cell lines, caco2 and hct116, which were treated with iasiii to assess ic50s. shortterm and longterm exposure to low concentrations (1 &µ;m and 0.1 &µ;m) of iasiii in two separate experiments was implemented to analyze emt, microsatellite status and the methylation pattern of <em>sept9</em> promoter. as expected, after 20 days of exposure to iasiii, the expression of <em>cdh1 </em>was significantly decreased while the expression of <em>cdh2</em>, <em>fib1</em> and <em>vim </em>was increased in caco2 and hct116, a finding that confirmed emt induction. however, there was no detectable alteration in the size of microsatellites. as for the methylation pattern, <em>sept9</em> promoter was hypomethylated as a result of longterm exposure to 0.1 &µ;m iasiii in caco2. longterm exposure of hct116 to both concentrations could induce hypomethylation of <em>sept9</em> promoter. our findings indicate no linkage between emt induction and microsatellite status in iasiiitreated crc cell lines. for the first time, the current study has shown that the induction of emt by iasiii is linked with <em>sept9</em> promoter hypomethylation in caco2 and hct116 in a concentration and timedependent pattern.</div>